Objective: To examine whether inflammation is present in subjects newly diagnosed with Parkinson’s disease (PD).

Background: Evidence for the role of inflammation in PD has been growing. Brain inflammation has been observed in postmortem PD brains. Cross-sectional studies from living persons with PD show increased cytokines and chemokines and changes in circulating immune cells. PET studies and genetic studies also support the role of inflammation in PD. Several key gaps remain as to the impact of inflammation in the degenerative process, including the extent of immune activation in persons with PD early in the disease and whether increased pro-inflammatory signals predict more rapid clinical decline.

Method: In the present study, we enrolled subjects with de novo PD (n=58) and age-matched healthy controls (n=62). Inclusion criteria for PD subjects included a diagnosis for PD by UK Brain Bank criteria within 2 years and no prior treatment with PD medications. Subjects underwent clinical assessments, including demographics, medication history, neurological examination, Movement Disorder Society-United Parkinson’s Disease rating scale (MDS-UPDRS), among other scales. Subjects underwent comprehensive neurocognitive assessment that met requirements as a Level II diagnostic MCI assessment as recommended by the MDS task force. Blood was obtained for flow cytometry and cytokine/chemokine analyses. Subjects underwent DPA-714 imaging and lumbar puncture if eligible and consented.

Results: Baseline demographics and medical history were comparable between groups. PD subjects showed significant differences in University of Pennsylvania Smell Identification Test, Schwab and England Activities of Daily Living, Scales for Outcomes in PD autonomic dysfunction, and MDS-UPDRS scores. Cognitive testing demonstrated significant differences in the cognitive composite, executive function, and visuospatial ability at baseline. Initial PET showed increased DPA-714 signal in PD subjects compared to healthy controls. Analyses of cytokines, chemokines, and other inflammatory markers are currently in process.

Conclusion: Our data show significant cognitive differences in controls compared to de novo PD subjects. We also observed evidence for increased central inflammation in these subjects, based on DPA-714 imaging. Longitudinal follow-up is in process to determine whether the presence of inflammation is predictive of cognitive decline in this cohort.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/inflammatory-changes-in-subjects-with-de-novo-parkinsons-disease/